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作 者:张敬[1] 刘艺敏[1] 张军[2] 邱水强[3] 龙继贤[3] 蔡亚滨[3]
机构地区:[1]同济大学医学院预防医学教研室,上海200070 [2]同济大学医学院生物学教研室,上海200331 [3]同济大学医学院临床医学系98级学生,上海200072
出 处:《同济大学学报(医学版)》2002年第2期107-109,共3页Journal of Tongji University(Medical Science)
基 金:铁道部科技基金资助项目 (J2 0 0 0Z10 8)
摘 要:目的 研究维生素E拮抗三氧化二镍的细胞毒作用及机制。方法 采用体外细胞培养法测定在不同浓度的维生素E(2 5mol/L ,5 0mol/L ,10 0mol/L)作用下 ,体外染镍肺泡巨噬细胞的存活率及活力 ,同时观察细胞内活性氧的产生 ,以及过氧化氢酶 (CAT)和谷胱甘肽过氧化物酶 (GSH Px)活力的变化。结果 在体外染镍肺巨噬细胞中加入维生素E后可提高该细胞的存活率和活力 ,减少活性氧的产生 ,增强细胞内CAT ,GSH Px的活性 ,其中以 10 0μmol/L的维生素E的作用最为明显。 结论 镍可致细胞脂质过氧化 ,维生素E具有拮抗镍对肺泡巨噬细胞的细胞毒作用 ,可能与其抗氧化功能有关。Objective To study the effects of vitamin E on injured alveolar macrophages exposed to Ni 2O 3 in vitro.Methods The alveolar macrophages were cultured with exposure of Ni 2O 3 in vitro. Meanwhile, 25,50 and 100 μmol/L vitamin E were added into the media,respectively. The detections of active oxygen, activity of catalase (CAT) and glutathione peroxidase (GSH?Px) in alveolar macrophages were carried out. Besides, cell activity and survival rate of alveolar macrophages were also determined after being exposed to Ni 2O 3 in vitro.Results The results revealed that vitamin E could decrease mortality and increase survival activity of alveolar macrophages. The production of active oxygen was decreased, while CAT and GSH?Px activity were increased at the same time. Vitamin E at 100μmol/L dose had the most dramatic inhibitory effect.Conclusion Vitamin E can antagonize lipid peroxidation of alveolar macrophages induced by Ni 2O 3 and it is probably due to its antioxidant property.
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